胎蛋白a在大鼠主动脉血管老化中的作用

Ö. Barış
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摘要

目的:在本研究中,我们旨在探讨炎症反应和氧化应激增加引起的血管系统变化与自然衰老大鼠主动脉组织中胎蛋白a水平的关系。材料与方法:将16只Wistar白化大鼠平均分为年轻组和老年组。切除胸主动脉。采用实时聚合酶链反应法评估衰老对主动脉、增殖、氧化应激和炎症标志物的影响。进行组织学检查以证实与衰老有关的发现,并进行血清取样以测定胎儿素a水平。结果:老年组白细胞介素-6水平降低(分别为1.007和0.099倍);p = 0.000)。胎儿素- a与白细胞介素-6水平呈正相关(r=0.56;p = 0.03)。超氧化物歧化酶-1测定的抗氧化能力无显著差异,而氧化应激标志物在老年大鼠中显著升高(诱导型一氧化氮合酶:1比812.3倍;p = 0.006;内皮型一氧化氮合酶:分别增加0.98倍和3.65倍;p = 0.001)。胎儿素a与内皮型一氧化氮合酶存在中度负相关(r=-0.56;p = 0.024)。结论:血管衰老通过炎症反应引起细胞损伤。胎儿蛋白a可能提示早期血管损伤。
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The role of fetuin-A in vascular aging in the rat aorta
Objectives: In this study, we aimed to investigate the relationship between vascular system changes due to the increased inf lammatory response and oxidative stress with advanced age and fetuin-A levels in aortic tissues of a naturally aged rat model. Materials and methods: A total of 16 Wistar albino rats were equally divided into two groups as the young group and the elderly group. The thoracic aorta was excised. The effect of aging on the aorta, proliferation, oxidative stress, and inf lammation markers were evaluated using the real-time polymerase chain reaction method. Histological examination was performed to confirm the findings related to aging, and serum sampling was performed to determine fetuin-A levels. Results: Interleukin-6 levels were lower in the elderly group (1.007 vs. 0.099-fold decrease, respectively; p=0.000). There was a moderate, positive correlation between fetuin-A and interleukin-6 levels (r=0.56; p=0.03). There was no significant difference in the antioxidant capacity as assessed by superoxide dismutase-1, while the oxidative stress markers were significantly higher in elderly rats (inducible nitric oxide synthase: 1 vs. 812.3-fold increase, respectively; p=0.006; endothelial nitric oxide synthase: 0.98 vs. 3.65-fold increase, respectively; p=0.001). There was a moderate, negative correlation between fetuin-A and endothelial nitric oxide synthase (r=-0.56; p=0.024). Conclusion: Vascular senescence causes cell damage through inf lammatory responses. Fetuin-A may indicate early vascular damage.
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